LincRNA-Cox2 targeting miR-150 regulating the proliferation and apoptosis of chondrocytes in osteoarthritis

Background: Osteoarthritis (OA) is a joint disease characterized by progressive cartilage degradation and inflammation, but the detailed pathogenesis of OA is still unclear. Here, we aimed to investigate the role of LincRNA-Cox2 in OA progression and the potential mechanism. Methods: OA mouse model and IL-1β-induced injury of mouse chondrocytes were conducted. Si-Cox2 was transfected into chondrocytes for elucidating the effect of LincRNA-Cox2 on OA. qR-TPCR was used to detect the expression of LincRNA-Cox2 and miR-150. Cell proliferation and apoptosis were analyzed by MTT assay and Annexin V/PI stain respectively. Western blot was used to evaluate the protein levels in chondrocytes. Results: High levels of LincRNA-Cox2 were observed in both cartilage tissues of OA and IL-1β-treated chondrocytes. Knockdown of LincRNA-Cox2 promoted the proliferation and inhibited apoptosis of chondrocytes. Mechanically, LincRNA-Cox2 directly target to miR-150, acting as a ceRNA, and the effect of si-Cox2 on proliferation and apoptosis in chondrocytes was reversed by miR-150 inhibitor. Moreover, LincRNA-Cox2 had ability to activate wnt/β-catenin pathway to regulate chondrocytes proliferation and apoptosis. Conclusion: Silencing LincRNA-Cox2 plays a protective role in OA by enhancing the proliferation and suppressing apoptosis of chondrocytes, which was related with increase of miR-150 and activation of Wnt/β-catenin pathway.